Advanced Clinical Insights and Practice: Ischemic Heart Disease
This issue sees the debut of a new series of continuing education articles. The series, Advanced Clinical Insights & Practice, is designed to provide continuing education to an ever-expanding realm of paramedicine that needs more of it: the critical care transport paramedic. Secondly, and equally important, are the benefits that can be reaped by other certification levels reading this feature. For EMT-Basics and Intermediates, it will provide a great enhancement to your core knowledge, although most of the interventions discussed will be beyond your traditional scope. For paramedics, it will augment both your pathophysiological understanding and clinical assessment/management skills of diseases and injuries discussed. Ultimately though, it is hoped that anyone who reads these articles will become a better clinician. The next article will appear in the July issue.
CEU Review Form Advanced Clinical Insights & Practice: Ischemic Heart Disease (PDF)Valid until May 2, 2008
Ischemic heart disease (IHD) is the leading cause of death in the United States for both men and women. The worst manifestation of IHD is a myocardial event that leads to infarction and death. Up until the last five years or so, it was thought that primarily males suffered from IHD; however, the diagnosis of acute myocardial infarction (AMI) is becoming more common in women, with an incidence approaching that of males. Often, female patients with chest pain were diagnosed with panic attacks, anxiety, hormonal changes and other diagnoses. Today, IHD kills more women than breast cancer, but public outcry and recognition are much larger for the latter.
CASE STUDY
You are a critical care paramedic working with an EMT-Basic and CCRN nurse as part of a critical care transport team. Your team is activated as the station's alert tones go off. Data provided on your pager indicates a woman is experiencing an MI in a nearby urgent care center and is to be transported immediately to the sponsoring medical center's cardiac catheterization laboratory, where an interventional cardiac catheterization team and cardiologist will be awaiting your arrival. Within 15 minutes of your alert, you pull the mobile MICU unit up to the doors of the referring facility and walk into the emergency department. Your first impression of the patient reveals a diaphoretic, 145 kg woman in her mid 40's, who looks very anxious and uncomfortable. She is moving around in the bed, complaining of "stomach gas" that she can't pass. You glance at the bedside monitoring equipment, which shows a heart rate of 112 bpm, blood pressure of 128/86, MAP of 100 mmHg, SpO2 of 92% on 4 lpm. The bedside 3-lead ECG shows a sinus tachycardia without ectopy in Lead II. After speaking to the patient to ensure the adequacy of the airway, breathing and circulatory components, your CCRN partner begins to switch over monitors and you go to find the referring physician.
You learn that the patient has smoked two packs of cigarettes a day for the past 20 years, and suffers from HTN and COPD. She is not allergic to anything, and you only get a partial list of her medications. You review the 12-lead ECG and note ST elevation in V2, V3 and V4, with reciprocal changes in the inferior leads. The nursing staff has inserted two intravenous catheters, with one capped and the other infusing normal saline. A urinary catheter is also already in place. Finally, you learn that her cardiac enzymes, blood work and chest x-ray results will be sent electronically to the medical center and arrive much sooner than you will.
You and your partner quickly apply the pacing/defib pads, along with a portable 12-lead ECG, NIBP, SpO2 monitor and EtCO2 monitor, and hang a bag of normal saline to the capped IV site. You increase the oxygen to 15 lpm via mask, and secure the patient and equipment to your cot. After the family says their good-byes to the patient, you're out the door and on the way to the receiving hospital.
PATHOPHYSIOLOGY
Through epidemiology, common risk factors for IHD have been identified (see Table 1). The astute provider can anticipate IHD complications when a patient meets this profile. It is also necessary to have an understanding of how this disease develops inside the human body, as this science has evolved from what was initially believed.
The blood supply to the myocardium can be split up into vessels outside the heart that deliver blood to regions of the heart muscle, and vessels within the myocardium that deliver the blood to the working cells specifically. The reason this is important to know is that an MI evolves from the endocardial layer (the terminal portions of the blood vessels providing perfusion to the heart) to the epicardial layer. This helps explain why early in the progression of an AMI (hyperacute phase), there are minimal/no ST segment changes, since the endocardial layer does not contribute much to the pumping action of the heart, and thereby does not contribute much to the electrical ECG tracing. This is still a very dangerous time, as the endocardial layer of the ventricles becomes ischemic and/or infarcts, and there is a chance for papillary muscle damage or rupture because it is contiguous with the endocardial layer itself, resulting in AV valve damage.
Early pathological principles of the AMI focused on the theory that a small plaque embolus broke off from the wall of larger vessels and floated downstream until it became lodged in smaller vessels. Once the emboli lodged and caused cessation of blood flow distally, ischemia/infarct would result in that region of the heart.
The modern hypothesis is that an inflammatory process (atherosclerosis) causes damage to the intimal lining of the blood vessels and endothelial cells become damaged. Once injury occurs, intimal dysfunction and inflammation progress through the following pathophysiologic events:
- Blood platelets and serum lipoproteins migrate into the vascular wall due to this intima damage.
- As a result of the damage, macrophages and smooth muscle cells of the tunica media layer also migrate to the region and begin to proliferate.
- As the disease progresses, longitudinal fatty streaks develop in the lumen of the blood vessels. The blood vessel then weakens as intima and media are deprived of nutrients from the expanding plaque.
- In an attempt to "close off" the fatty streaks, smooth muscle cells produce collagen and migrate over the fatty streak to form a fibrous cap.
- Fibrous caps are not stable over time and have a tendency to rupture. This activates the body's clotting mechanism with development of a thrombus that occludes the blood vessel.
If the vessel subjected to this phenomenon is one of the coronary arteries, upon rupture of the fibrous cap and resultant thrombus formation, an AMI can easily result. Identification of this AMI is based on a combination of three factors: the patient's clinical presentation, cardiac enzyme changes and ECG findings. The ECG is especially valuable to the clinician (beyond providing confirmatory ECG evidence of an ischemic or infarction episode), as it helps identify the wall(s) of the heart affected by the event. The knowledge of what part of the heart is damaged allows the critical care medic to anticipate additional complications that may develop. To fully appreciate this, understanding basic coronary anatomy is necessary.
CORONARY PERFUSION
The heart has two main coronary arteries originating from the base of the aorta: right and left. The right coronary artery perfuses the right atrium, right ventricle and a portion of the left ventricle. The right coronary artery usually gives rise to the posterior descending artery that perfuses the posterior wall and inferior wall of the left ventricle, and also perfuses the SA node and AV node in the majority of patients. Soon after leaving the aorta, the left coronary artery splits into two main branches: the left anterior descending (LAD) and left circumflex (LCX). The LAD perfuses the ventricular septum, the anterior wall of the left ventricle and a portion of the heart's apex. The LAD also perfuses the heart's conduction system embedded within the septal wall—the bundle branches. The LCX goes on to perfuse the lateral wall of the left ventricle and usually terminates in the posterior region of the left ventricle.
Understanding coronary artery anatomy allows the critical care team to correlate ischemic/infarction findings on the 12-lead ECG with the coronary artery involved. It is traditionally accepted that it requires two anatomically contiguous leads of the ECG that view the same wall of the heart to show electrical changes consistent with an AMI (ST segment changes >1mm) in order to suspect a certain coronary blood vessel is occluded. Table II summarizes these findings.
CLINICAL CONSEQUENCE
Merely understanding the above discussion is pointless without applying it to your patient assessment and management. Remember, the determination of a coronary ischemic or infarction episode is based on three categories of information. First, the clinical presentation of the patient (objective and subjective). At this point, the critical care paramedic should be well versed in the clinical presentation (symptomatology) of an ischemic event. Second, the use of bedside cardiac enzyme marker tests, which are becoming increasingly popular with both prehospital and critical care transport providers. Third, 12-lead ECG findings. The presence of ischemic changes in two or more anatomically contiguous leads is considered evidence of a cardiac event. Remember, however, individually, each of these categories may not show confirmatory evidence of an AMI even if one is progressing. Recall that patients with chronic peripheral vascular disease (such as long-term diabetics) may not have chest pain due to peripheral neuropathy. Additionally, cardiac enzyme release into the bloodstream from the damaged cardiac cells may not be at a level considered elevated at time of sampling. Finally, there are other electrical events that may be concurrently present in the 12-lead that can hide (or mimic) changes indicative of an AMI. The lesson is to always have a high index of suspicion.
Should an ischemic event be occurring, it's best for the critical care team to simultaneously treat the patient's current condition, as well as anticipate future complications. For example, if a wall of the left myocardium is failing, stroke volume and cardiac output may be diminished, which may result in sympathetically mediated tachycardia that can further hamper cardiac output if the diastolic filling phase of the ventricles becomes too short. Further complicating this is that the coronary arteries are only perfused during diastole, so shorter diastolic phases translates into diminished coronary perfusion. Because of this, critical care providers often administer beta blockers to patients with an AMI, as long as there is not concurrent bradycardia.
It is also important to understand that an ischemic event can affect more than the contractile muscle cells. If the conduction system is deprived of oxygenated blood, it too can falter and fail during a cardiac event. If the critical care paramedic identifies a septal or anterior wall event from LAD occlusion, it may also result in bundle branch blocks and infranodal heart blocks that typically do not respond to administration of atropine. An inferior wall MI, indicative of right coronary artery occlusion, may also cause nodal heart blocks or sinus bradycardias if the occlusion is located in the proximal portion of the right coronary artery. In addition, the use of drugs during an MI that result in peripheral vasodilation (e.g., nitro) could be detrimental to a right ventricular MI from a drop in central venous pressure. (Remember that central venous pressure preloads the right side of the heart.) This is why right ventricular views must be obtained whenever there is evidence of inferior wall infarctions on a 12-lead. In this instance, it is common practice to administer fluids prior to vasodilatory drugs. If the patient with an inferior wall infarction shows right ventricular involvement, it is not uncommon to administer 1 to 2 liters of normal saline prior to vasodilatory drugs. Following the infusion, carefully administer the nitrates and/or narcotics so that a significant drop in blood pressure does not occur from this afterload reduction.
Other complications include changes in automaticity from ischemic cells of the heart resulting in dysrhythmias. The patient could experience valvular dysfunction resulting in acute pulmonary edema, or even ventricular rupture as the infarcted tissue becomes weak and tears in response to the pressure generated during ventricular systole.
CRITICAL CARE MANAGEMENT
Myocardial ischemia is a deficiency of oxygen to the heart. The management goal is simple: get more oxygenated blood to the myocardium. (While oxygenating a patient is an easy concept for a paramedic to grasp, promoting reperfusion is often not a topic discussed at great lengths.) There are primarily two ways to bust clots and reperfuse the ischemic area: fibrinolytic therapy and percutaneous balloon angioplasty. Both interventions are usually carried out at facilities capable of handling the complications of these therapies, and critical care providers are often needed to transport these patients to the appropriate tertiary medical facility.
During transport, always optimize oxygenation to the cardiac patient. Remember, the goal is to provide the highest amount of oxygenated perfusion to the ischemic regions. In order to do this, supply every patient with supplemental oxygen. If the SpO2 is at or above 90% according to the American Heart Association, the patient can be placed on low-flow (2–4 lpm) oxygen. If oxygen saturation is less than this, or in situations of complicated MIs or unrelenting chest pain, the patient should be placed on high-flow oxygen (12–15 lpm). Once the oxygenation status has been assured, the critical care paramedic should turn his/her attention to the perfusion status.
Critical care transport teams will often encounter nitroglycerin infusions that have been initiated by the referring facility. It is also common for critical care paramedics to initiate a nitro infusion themselves on a patient who is unresponsive to sublingual nitro. Nitroglycerin is a very powerful drug that can manipulate preload and myocardial oxygenation status, as well as blood pressure. Nitroglycerin infusions are commonly started after the patient has received three sublingual nitro pills/sprays, is still complaining of cardiac pain, and is not precluded by a low systolic pressure. The infusion is started at 5–10 mcg/min and titrated every 10 minutes in response to the patient's pain level and blood pressure. Because nitroglycerin, through a series of reactions, allows for further release of endogenous nitrous oxide, the result is enhanced venodilatation and epicardial vessel dilatation. This further promotes a decrease in preload, a drop in systolic pressure, and diminishment in the workload the heart has to maintain (all leading to a decrease in myocardial oxygen consumption). The nitroglycerin infusion is commonly titrated up to 150–200 mcg/min (or a pain-free state) as long as the patient remains hemodynamically stable.
Another important medication that can be administered to an infarcting patient is a beta blocker. During an infarction, the body releases large quantities of endogenous catecholamines that cause an increase in heart rate and contractile force, both of which increase MVO2 (the heart's demand for oxygen) and spread the size of the infarct. The goal through this treatment is to lower the heart rate to 50–60 bpm. Administration of this class of drugs blocks the beta adrenergic receptor sites, thereby diminishing the effects of heightened sympathetic tone typically present. Metoprolol is the recommended beta blocker at an initial dose of 5 mg IVP (providing the patient is not bradycardic). This dose is repeated every five minutes to a total of 15 mg. Metoprolol is preferred because it is a beta 1 specific blocker, meaning it will primarily affect the adrenergic receptors in the heart that result in a decrease in chronotropy (rate), inotropy (force) and dromotropy (electrical conduction velocity). Obvious precautions or contraindications to metoprolol are a bradycardic rate or patients displaying AV node heart blocks.
Pain relief is a priority concern during transport. The clinical endpoint in the management of chest pain should be a pain level of "0". More simply stated, as long as the patient complains of any chest pain (and the systolic BP does not preclude it), treat it! Obviously, with increased pain, there can be an increase in the infarct spreading, as previously described. Traditionally, morphine sulfate had been used for ongoing pain management because it was the standard pain medication used by ED physicians. Since they were often included in the creation of prehospital protocols, prehospital treatment included that intervention as well. Although morphine is a potent analgesic, it also decreases preload through the release of histamines. This further drop in systolic pressure is often an unwanted side effect (remember that nitroglycerin administration will drop blood pressure, as will the metoprolol). To further enhance pain relief without the same drop in blood pressure, many clinicians have switched to a synthetic opiate known as fentanyl. It is 100 times more potent than morphine; however, it has a shorter half-life and does not promote the same degree of hypotension. Additionally, since it is short acting, the patient's mental status will return to normal faster should the receiving physician have questions when they arrive in the ED, ICU or cath lab. Normal dosages for fentanyl are 25–50 mcg IVP, with a total dose of 200–300 mcg, as long as the patient remains hemodynamically stable.
Aspirin is a common therapy for cardiac patients both in and out of the hospital, and a proven lifesaver in large groups of study patients. Almost all patients have already received their ASA dosage before arrival at the ED or transport by the critical care team; however, check to make sure that this valuable medication wasn't accidentally overlooked. ASA is an anti-platelet medication that prevents further "sticking" to the clot formed in the coronary artery at the site of occlusion. The dosage is usually one baby ASA 81 mg chewed for immediate release and one 81 mg swallowed if the patient has no contraindications (some protocol allows up to four aspirin).
If the patient is picked up from the ED, there may be other anti-platelet medications infusing, especially when the patient is going to be transferred to the cardiac catheterization laboratory. Glycoprotein IIb–IIIa receptors are the final (and most common) pathway by which platelets aggregate at the site of injury. Because all platelets have to bind at one of these sites, use of a medication that prevents further binding can almost ensure the clot formation will not progress any further. Common IIb–IIIa receptor inhibitors include ReoPro (abciximab) and Integrilin (eptifibatide), both of which are administered via a continuous IV infusion. In addition, a heparin infusion or an injection of unfractionated heparin may have been previously given to prevent the conversion of fibrinogen to fibrin, further inhibiting clot formation.
CONCLUSION
Prehospital ALS providers or the referring medical facility will often call upon critical care paramedics to treat and transport the cardiac patient when the patient's condition exceeds the care readily available. Many times the patient will have already received traditional medications of oxygen, ASA, nitro and morphine. It is the responsibility of the critical care paramedic to consider ongoing management options for pain relief and systolic blood pressure regulation given the medication administered thus far, the area(s) of the heart damaged by the AMI and the overall clinical presentation. The thoughts that should be guiding the critical care paramedic's actions include how to better ensure oxygenation, how to promote better myocardial perfusion while diminishing myocardial workload, and how to limit or stop thrombus formation. To achieve this, the critical care paramedic often has access to additional drugs that are beyond the prehospital paramedic's scope. These drugs can be as detrimental as they are helpful if improperly employed. It is the responsibility of the critical care paramedic to stay abreast of current AMI management and utilize medication as the patient's condition warrants.
CEU Review Form Advanced Clinical Insights & Practice: Ischemic Heart Disease (PDF)Valid until May 2, 2008
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Randall W. Benner, Med, MICP, NREMT-P, is an instructor in the Department of Health Professions at Youngstown (OH) State University, and has over 20 years of experience in the delivery of prehospital medicine, critical care transport medicine and prehospital education. He currently serves as the director of the Emergency Medical Technology Program at Youngstown State University, where he is responsible for all levels of prehospital EMS and critical care educational programs. While still functioning actively as a prehospital provider and flight paramedic in Ohio, he is also completing his PhD in Education.
Matthew S. Zavarella, RN, NREMT-P, MS, CFRN, CCRN,CEN, SRNA, a practicing paramedic/nurse, has been involved with EMS, EMS education, publishing and aeromedical critical care transport for 15 years. He holds a bachelor's in Health Sciences from YSU and a master's in Science from the University of Mississippi Medical Center. He's also nearing completion of a second master's degree in Nursing Anesthesia from the Excela Health School of Anesthesia in Latrobe, PA. He works part time as a critical care nurse and a critical care flight nurse.
